Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interaction between pancuronium, d-tubocurarine, polymyxin B, and neostigmine was studied in the rat diaphragm-phrenic nerve preparation. Polymyxin B (5 mug/ml) did not affect twitch tension alone but decreased the pancuronium ED50 from 0.8 mug/ml to 0.32 mug/ml and the d-tubocurarine ED50 from 0.25 mug/ml to 0.15 mug/ml. Neostigmine (0.2 to 10 mug/ml) antagonized pancuronium or d-tubocurarine-induced depression of twitch tension. In contrast, neostigmine (0.001 to 0.2 mug/ml) augmented polymyxin B depression. Similarly, neostigmine (0.1 mug/ml) augmented combined polymyxin B-pancuronium or polymyxin B-d-tubocurarine depression of twitch tension. The authors conclude that polymyxin B potentiates the neuromuscular blockade from pancuronium or d-tubocurarine and that neostigmine further augments this block.
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PMID:The interaction between d-tubocurarine, pancuronium, polymyxin B, and neostigmine on neuromuscular function. 17 4

Dose-response relationships for doxacurium and neostigmine were established in 24 young (18-40 yr) and 24 elderly (70-85 yr) patients, ASA physical status I or II, anesthetized with thiopental, fentanyl, nitrous oxide, and isoflurane. Mechanomyographic response of the adductor pollicis muscle to the train-of-four stimulation of the ulnar nerve was recorded. Doxacurium (5, 10, 15, or 20 micrograms/kg IV) was administered by random allocation. After maximal blockade, and additional dose, for a total of 30 micrograms/kg, was administered. When first twitch height recovered to 25%, incremental doses of 5 micrograms/kg were administered for maintenance of relaxation. Neostigmine (5, 10, 20, or 40 micrograms/kg) was injected at 25% first twitch recovery, and neuromuscular monitoring was continued for 10 min. The doses of doxacurium (+/- SEM) required to produce a 50%, 90%, and 95% depression of twitch tension in the young patients were, respectively, 13.3 +/- 1.6, 23.6 +/- 2.8, and 28.6 +/- 3.4 micrograms/kg, not statistically different from corresponding values in the elderly, 11.8 +/- 1.3, 21.2 +/- 2.3, and 25.9 +/- 2.9 micrograms/kg, respectively. Time to 25% recovery after 30 micrograms/kg was 80.2 +/- 12.2 min in the young versus 133.0 +/- 17.1 min in the elderly (P less than 0.05). Neostigmine-assisted recovery was not significantly different in both groups. The estimated doses of neostigmine to obtain 70% train-of-four recovery after 10 min were 53.6 +/- 7.5 micrograms/kg in the young and 41.6 +/- 5.8 micrograms/kg in the elderly (P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dose-response relations of doxacurium and its reversal with neostigmine in young adults and healthy elderly patients. 153 72

Twenty anephric and 20 healthy patients received a bolus dose of mivacurium 150 micrograms kg-1. When the first EMG response (T1) of the train-of-four had recovered to 5% of control (T0), an infusion of mivacurium 10 micrograms kg-1 min-1 was started and adjusted to keep T1 at 5%. Ten patients in each group were given neostigmine 35 micrograms kg-1 when the infusion was stopped when T1/T0 had recovered to 20%; in the others recovery was spontaneous. After the bolus dose of mivacurium, mean (SD) depression of T1 was greater in the anephric group than in the normal group (98.4 (3.5) vs 96.8 (4.4)%; P less than 0.01) and recovery of T1/T0 to 5% was slower (15.3 (6.9) vs 9.8 (3.5) min; P less than 0.01). Anephric patients required a slower infusion rate (6.3 (1.9) vs 10.4 (2.8) micrograms kg-1 min-1; P less than 0.001). Neostigmine hastened recovery of both T1/T0 and T4/T1 in both groups. Spontaneous recovery of T1/T0 (from 25% to 75%) after the infusion was also slower in anephric patients (12.2 (8.2) vs 7.7 (1.2) min; P less than 0.05). Plasma cholinesterase activity was less in the anephric group (785 (207) vs 943 (217) iu litre-1; P less than 0.05) and there was a (negative) correlation overall between cholinesterase activity and time to 5% recovery of T1/T0 after the bolus dose (r = -0.42; P less than 0.02). We conclude that patients with chronic renal failure may require a reduced dose of mivacurium.
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PMID:Use of mivacurium chloride by constant infusion in the anephric patient. 164 38

The role of central nervous system (CNS) cholinergic and noradrenergic mechanisms in the pathogenesis of depression and hypothalamic-pituitary-adrenal (HPA) axis hyperactivity is examined using the Behavioral Despair rat model of depression. Immobility (IM), the analog of depression in this model, and plasma corticosterone (C) were increased by physostigmine (PHYSO). Neostigmine (NEO), which does not cross the blood-brain barrier, produced the same peripheral cholinomimetic effects and motor inhibition as PHYSO, but did not change IM. PHYSO's effects on C and IM were blocked by metoprolol pretreatment and partially blocked by clonidine pretreatment. PHYSO increased acetylcholine in the striatum. In this animal model of depression, cholinergic and noradrenergic mechanisms are interactively involved in the regulation of behavioral depression and the HPA axis.
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PMID:The cholinergic-adrenergic hypothesis of depression reexamined using clonidine, metoprolol, and physostigmine in an animal model. 184 8

Acetylcholinesterase inhibitors produce diverse physiologic effects, but lethal exposure consistently produces respiratory failure due to neuromuscular paralysis or depression of respiratory control centers in the medulla. Simultaneous measurement of gastrocnemius muscle contraction and efferent phrenic nerve activity was used to determine the primary cause of respiratory failure produced by neostigmine and diisopropyl fluorophosphate (DFP) in anesthetized cats. Both neostigmine and DFP abolished phrenic nerve activity prior to producing neuromuscular blockade. Furthermore, neostigmine did not alter brain acetylcholinesterase activity and pretreatment with either atropine methylbromide or atropine increased the dose of neostigmine required to abolish phrenic nerve activity. In contrast, DFP abolished brain cholinesterase activity and only atropine inhibited its respiratory effects. Despite the loss of efferent phrenic nerve activity, there is no evidence of a direct effect of neostigmine on respiratory control centers. Neostigmine may instead alter afferent inputs which modulate respiration to produce a reflex respiratory failure.
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PMID:Mechanisms of respiratory failure produced by neostigmine and diisopropyl fluorophosphate. 206 14

The use of vecuronium in six patients with myasthenia gravis undergoing thymectomy is described the train-of-four twitch technique was used to monitor neuromuscular function. The first two patients received an initial dose of 0.02 mg/kg and incremental doses of 4 micrograms/kg, which is in the order of one fifth of that normally used. Satisfactory depression of the first twitch of the train-of-four, however was not obtained and, therefore, in the remaining four patients the doses were doubled. At this dose satisfactory depression of the first twitch was achieved. Neostigmine 5.0 mg produced adequate reversal of residual neuromuscular blockade and the train-of-four twitch response recovered to normal levels. With reduced dosage and with careful neuromuscular monitoring, vecuronium can be used safely in the myasthenic patient.
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PMID:Vecuronium in the myasthenic patient. 286 78

The ability of edrophonium and neostigmine to antagonize nondepolarizing neuromuscular blockade produced by steady-state infusions of atracurium, pancuronium, and vecuronium was studied in 71 adult patients anesthetized with nitrous oxide and halothane. Infusion rates of blocking drugs were adjusted so that single twitch depression as measured by the evoked integrated EMG of the hypothenar muscles was kept at 10% of control. Two minutes after the termination of the infusion either edrophonium (0.75 mg/kg) or neostigmine (0.05 mg/kg) was administered. Single twitch depression and train-of-four (T4/T1) fade was recorded during the recovery period. T4/T1 fade ratios observed at 20 min postreversal were 0.80 (atracurium-edrophonium); 0.76 (vecuronium-edrophonium); 0.44 (pancuronium-edrophonium); 0.95 (atracurium-neostigmine); 0.89 (vecuronium-neostigmine); and 0.68 (pancuronium-neostigmine). Under conditions of this study neostigmine produced more rapid and complete recovery than did edrophonium. Although edrophonium produced adequate antagonism of atracurium if 20-30 min were allowed to elapse, edrophonium reversal of pancuronium was rarely acceptable even at 30 min. Increasing the dose of edrophonium to 1.0 mg/kg produced single twitch values of 0.90 at 5 min postreversal but did not increase the rate of recovery of the train-of-four fade ratio. Neostigmine reversal of pancuronium, on the other hand, generally produced T4/T1 ratios of greater than 0.70 in 20-30 min. Although the pattern of recovery seen after reversal of vecuronium was in general quite similar to that seen after atracurium, two patients in the vecuronium-edrophonium group showed delayed recovery and also failed to respond significantly to subsequent doses of neostigmine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recovery times following edrophonium and neostigmine reversal of pancuronium, atracurium, and vecuronium steady-state infusions. 287 31

In a double-blind, prospective, randomised trial in 30 women undergoing laparoscopy, atracurium and vecuronium were compared in equipotent (2 X ED95) doses. In the atracurium group, first twitch depression was significantly greater at one minute, and degree of fade significantly greater at one and two minutes, but thereafter neuromuscular monitoring showed no significant difference between the groups. Clinically there was no significant difference between the drugs. Mild intraoperative hypotension was equally common in both groups as was sinus bradycardia. Reversal and recovery were comparable in the two groups. Neostigmine was required in all patients and in three (one atracurium, two vecuronium) a second dose was required in all patients and in three (one atracurium, two vecuronium) a second dose was administered on clinical grounds. Antagonism of the neuromuscular block is required with surgery of this duration despite the intermediate duration of action of the relaxant drugs.
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PMID:A clinical comparison of atracurium and vecuronium in women undergoing laparoscopy. 288 97

Neostigmine 1.25 mg or 0.625 mg was used to antagonize neuromuscular blockade produced by either atracurium 0.5 mg kg-1 or vecuronium 0.1 mg kg-1 in four groups of patients (n = 45) when the first EMG response of the train-of-four (A') had recovered to 10% of control (A). The time for A'/A and the train-of-four ratio (D'/A') to reach 70% was recorded. It was found that, after both atracurium and vecuronium, neostigmine 1.25 mg considerably accelerated recovery and, when compared with previous results, differed little from neostigmine 5.0 mg or 2.5 mg. Neostigmine 0.625 mg also significantly accelerated recovery after atracurium and was comparable to neostigmine 1.25 mg. However, with neostigmine 0.625 mg after vecuronium, recovery of D'/A' (but not A'/A) was little faster than spontaneous. Neostigmine 1.25 mg appears to be almost as effective as neostigmine 5.0 mg or 2.5 mg in antagonizing considerable block (90% depression of twitch height) produced by either atracurium or vecuronium, but neostigmine 0.625 mg is not sufficient, especially after vecuronium.
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PMID:Antagonism of blockade produced by atracurium or vecuronium with low doses of neostigmine. 290 46

Relatively high concentrations of verapamil or EGTA [ethylene glycol-bis (beta-aminoethyl ether) N, N, N',N'-tetra acetic acid] inhibit contraction (P) of the rat phrenic nerve-hemidiaphragm preparation elicited by direct or indirect stimulation. The inhibitory effect of verapamil is greater (P less than 0.002) with direct (I50 = 26.3 +/- 1.7 microM) than indirect = I50 = 37.6 +/- 1.9 microM) stimulation. For EGTA the reverse is true: I50 is 1320 +/- 80 microM with direct and 1100 +/- 60 microM with indirect stimulation. The greater than 90% verapamil-induced depression of P can only be partially reversed by washout. Increasing the [Ca2+] or the addition of 4-aminopyridine (4AP) has insignificant antagonist effect. Except for the antagonism by 4AP during direct stimulation, the EGTA-induced depression of P is better antagonized by washout, increase of the [Ca2+], or the addition of 4AP than that caused by verapamil. Neostigmine did not antagonize the depression of P caused by either verapamil or EGTA. The findings presented indicate that the primary site of action of verapamil is postjunctional and that of EGTA is prejunctional.
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PMID:The effect of verapamil and EGTA on the rat phrenic nerve-hemidiaphragm preparation. 298 88


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